期刊论文详细信息
FEBS Letters
Activation of ryanodine receptor/Ca2+ release channels downregulates CD38 in the Namalwa B lymphoma
Mackrill, John J.1  McCarthy, Tommie V.1  Datar, Sue1 
[1] Department of Biochemistry, Biosciences Institute, National University of Ireland, University College Cork, College Road, Cork, Ireland
关键词: CD38;    Lysosome;    Ca2+;    Cyclic ADP ribose;    Ryanodine receptor;    ALLM;    N-acetyl-Leu-Leu-Met-al;    cADPr;    cyclic ADP ribose;    cGDPr;    cyclic GDP ribose;    CmC;    4-chloro-meta-cresol;    Fluo-3AM;    fluo-3-acetoxymethyl ester;    KHB;    Krebs–Henseleit buffer;    MG132;    Z-Leu-Leu-Leucinal;    NAD;    nicotinamide adenine dinucleotide;    NGD;    nicotinamide guanine dinucleotide;    RT-PCR;    reverse transcription polymerase chain reaction;    RyR;    ryanodine receptor;   
DOI  :  10.1016/S0014-5793(03)01122-0
学科分类:生物化学/生物物理
来源: John Wiley & Sons Ltd.
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【 摘 要 】

CD38 is a multifunctional ectoenzyme that catalyses formation of cyclic ADP ribose (cADPr), a second messenger that opens ryanodine receptor (RyR) Ca2+ channels. Despite its importance in signal transduction processes, little is known about the mechanisms regulating CD38 expression levels. In the current study, ryanodine stimulation of Ca2+ release in Namalwa cells decreased both CD38 protein abundance and cyclase activity. Reductions in cyclase activity were prevented by RyR antagonists, by lysosomal blockers, though not by calpain or proteasomal inhibitors. These findings indicate a novel negative feedback mechanism between RyR channel activity and CD38 abundance acts in cADPr signal transduction.

【 授权许可】

Unknown   

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